Vasodilation and Vasoconstriction: Reality Check

What is vasodilation? Definition of vasodilation

Vasodilation
(definition) = the increase in the internal diameter of blood vessels that is
caused by relaxation of smooth muscle within the wall of the vessels, thus
causing an increase in blood flow. The opposite effect is vasoconstriction.

During vasodilation, when blood vessels dilate, the blood flow is
increased due to a decrease in vascular resistance. However, for practical
purposes, dilation of arteries and arterioles has the most significant
therapeutic value since these blood vessels are the main contributors to
systemic-vascular resistance and, therefore, dilation of arteries and arterioles
leads to an immediate decrease in arterial blood pressure and heart rate. Hence,
chemical-arterial dilators are used to treat heart failure, systemic and
pulmonary hypertension, and angina. Dilation of venous-blood vessels decreases
venous-blood pressure. Such agents can be used to reduce cardiac output,
venous-and-arterial pressure, tissue edema (due to better capillary-fluid filtration),
and myocardial oxygen demands. Let us consider, unlike useless official medical
sources, practical or real-life aspects of vasodilation and
vasoconstriction.

Among arterial dilators,
the natural vasodilation agent CO2 is probably the
most powerful chemical. The vasodilation effect is present in healthy people
due to normal arterial CO2 concentration. According to Dr.
M. Kashiba, MD and his medical colleagues from the Department of Biochemistry and
Integrative Medical Biology, School of Medicine, Keio University in Tokyo, CO2
is a "potent vasodilator" (Kashiba et al, 2002),
while Dr. H. G. Djurberg and his team from the
Department of Anesthesia, Armed Forces Hospital, in Riyadh, Saudi Arabia
wrote that "Carbon dioxide, a most potent cerebral vasodilator..."
(Djurberg et al, 1998).

Since CO2 is the most potent vasodilator, vasoconstriction should be a
problem for those people who suffer from arterial hypocapnia. This relates to
people with hyperventilation (or breathing more than the medical norms)
and a normal or nearly normal ventilation-perfusion ratio (e.g., no problems with lungs).
Indeed, people with, for example, COPD, may hyperventilate, but their blood CO2
is generally higher than normal. Here are some studies that explain blood flow
and vasodilation/vasoconstriction in the healthy and sick people.

Note that advanced stages of some conditions (e.g., asthma and CF) can lead to lung destruction, ventilation-perfusion mismatch and arterial hypercapnia causing further reduction in body oxygen levels.

However, there are solid physiological reasons why first creatures with lungs that existed more than 2 million years ago did not suffer from CO20related vasodilation due to one environmental factor. The explanation to this curious fact is provided below as yur bonus content. This factor also explains why hyperventilation was useful and efective in order to get more oxygen in cells of the body.

What is the physiological
mechanism of the reduced blood flow to vital organs? Arteries and arterioles
have their own tiny smooth muscles that can constrict or dilate
(causing vasodilation)
depending on CO2 concentrations. When
we breathe more, our arterial CO2 level
becomes smaller, blood vessels constrict and vital organs (like the
brain, heart, kidneys, liver, stomach, spleen, colon, etc.) get less
blood supply. Similarly, hypocapnia causes spasm of all other smooth
muscles of the human body: airways or bronchi and bronchioles,
diaphragm, colon, bile ducts, etc.

This effect explains why sick people have less blood going to their brains,
heart, liver, and other vital organs. A normal
breathing pattern provides people with normal perfusion and
oxygen supply for all vital organs due to CO2 vasodilation.
However, since modern people breathe more than the medical
norm (hyperventilate), they have to suffer from CO2-deficiency effects.

Are there any related systemic effects? The state of these
blood vessels (arteries and arterioles) define total resistance to the
systemic blood flow in the human body. Hence, hypocapnia increases
strain on the heart. Normal CO2 parameters make resistance to blood
flow in the cardiovascular system small. Hence, breathing directly
participates in regulation of the heart rate. The father of
cardiorespiratory physiology, Yale University Professor Yandell
Henderson (1873-1944), investigated this effect about a century ago.

Among his numerous physiological studies, he performed
experiments with anaesthetized dogs on mechanical ventilation. The
results were described in his publication "Acapnia and shock. - I.
Carbon dioxide as a factor in the regulation of the heart rate". In
this article, published in 1908 in the American Journal of Physiology,
he wrote, "... we were enabled to regulate the heart to any desired
rate from 40 or fewer up to 200 or more beats per minute. The method
was very simple. It depended on the manipulation of the hand bellows
with which artificial respiration was administered... As the pulmonary
ventilation increased or diminished the heart rate was correspondingly
accelerated or retarded" (p.127, Henderson, 1908).

Be observant. When you get a small bleeding cut or a wound,
deliberately hyperventilate and see if that can help stop the bleeding.
It should due to vasoconsctriction.
As an alternative, perform comfortable breath holding and
breathe less and accumulate CO2. What would happen with your bleeding?
(It should increase due to vasodilation.) Now you know
what to do after dental surgeries,
brain traumas, and other accidents involving bleeding. It is natural
for humans and other animals to breathe heavily in such conditions.
Hence, hyperventilation can be life-saving in cases of severe bleeding.

As many health professionals found, blood flow to vital organs
is directly proportional to blood CO2 concentrations. Consider this example of
vasodilation - vasoconstriction. According to the Handbook
of Physiology (Santiago & Edelman, 1986), cerebral
blood flow decreases 2% for every mm Hg decrease in CO2 pressure. When
people have 20 mmHg CO2 in their blood (half of the official norm),
they have about 40% less blood supply to the brain in comparison with
normal conditions. Only skeletal muscles can get more blood in
conditions of hyperventilation.

Personal experiment. Take 100 deep and fast breaths
through the mouth and you can pass out due to ... lack of oxygen and
poor blood supply for the brain. Why? Because CO2 is a vasodilator
(dilator of blood vessels).

Note that there is another powerful chemical NO (nitric oxide) that is
also able to produce vasodilation, while its lack causes
vasoconstriction. Humans generate nitric oxide in sinuses
and, hence, mouth breathing prevents us from inhaling our own nitric oxide
(see web page: Nasal Nitric Oxide
Effects). Meanwhile, as some medical studies claim, CO2 is a most
powerful known vasodilator.

YouTube Video about CO2 - Vasodilation-Vasoconstriction effect

A first part of this video clip explains how and why voluntary
forceful hyperventilation leads to fainting: when we start to breathe
heavily, CO2 content in the arterial blood sharply falls within seconds and
blood vessels (arteries and arterioles) constrict since CO2 is the key
factor in vasodilation.